Morbidity in schistosomiasis is caused by the host response to schistosome eggs which a deposited in the venous system and carried to the tissues. Pathology is proportional to the number of eggs laid and it is thus important to understand factors underlying worm fecundity and the extent to which fecundity is reflected by eggs passed in the feces, the measurable indicator of infection intensity in humans. The rate of destruction of S. mansoni or S. japonicum eggs in the tissues of mice has proved to be so slow as to make it a negligible factor in calculating the fecundity of schistosomes. The fecundity (essentially = to eggs/day passed in the feces + eggs/day accumulated in the tissues) of S. mansoni in mice infected with a single pair of worms averages about 330 eggs/day/female and eggs passed in the feces reflect the intensity of egg laying in individual mice over a 1 year period of infection. S. japonicum lays over 2000 eggs/day/female early in infection but the rate of egg laying decreased with increased duration of infection to less than 1000 eggs/day/female 1 year after infection. The number of eggs in the feces decreases in parallel to the decrease in total egg laying. The fecundity of S. mansoni but not S. japonicum is decreased in SCID mice. S. mansoni frequently fails to mature in nude mice but worms which mature produce The objectives of this project are to define and generate filarial proteins that are important in inducing parasite-specific immune responses in the human host and to understand, at a molecular level, the differences among related filarial species. Recombinant antigens and probes have been identified that: a) encode immunoreactive and potentially protective molecules of W. bancrofti; b) can distinguish among related filarial species; c) identify repeated segments of either the W. bancrofti genome or that of Loa loa; d) may be of potential diagnostic importance; and e) induce immediate hypersensitivity type responses in lymphatic filarial syndromes.